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Protein kinase inhibitors as sensitizing agents for chemotherapy
- Available as
- Online
Details
- Creator
- edited by Zhe-Sheng Chen and Dong-Hua Yang
- Format
- Books
- Language
- English
- Contributors
- Publication
-
- First edition
- London, United Kingdom : Academic Press, an imprint of Elsevier, [2019]
- ©2019
- Physical Details
-
- 1 online resource (294 pages)
- ISBNs
- 9780128164358, 9780128127384, 0128127384, 0128164352
- OCLC
- on1076269079
- Front Cover -- Protein Kinase Inhibitors as Sensitizing Agents for Chemotherapy -- Copyright -- Contents -- Contributors -- About the Editors -- A: Certifications, Honors, Awards, and Other Recognitions -- Research Interests -- About the Series Editor -- Aims and Scope for Series ``Cancer Sensitizing Agents for Chemotherapy´´ -- Preface -- Chapter 1: EGFR and HER2 Inhibitors as Sensitizing Agents for Cancer Chemotherapy -- Introduction -- Tyrosine Kinases: Targeting the EGFR and HER2 Receptors -- Resistance to Chemotherapy -- EGFR and HER2 Inhibitors as Sensitizing Agents to Chemotherapy -- Gefitinib -- Erlotinib -- Lapatinib -- Afatinib -- Pelitinib -- Osimertinib -- Conclusion -- Acknowledgments -- References -- Chapter 2: BCR-ABL Inhibitors as Sensitizing Agents for Cancer Chemotherapy -- Introduction -- BCR-ABL Inhibitors as Sensitizing Agents for Cancer Chemotherapy -- Imatinib as Sensitizing Agent for Cancer Chemotherapy -- Nilotinib as a Sensitizing Agent for Cancer Chemotherapy -- Dasatinib as a Sensitizing Agent for Cancer Chemotherapy -- Ponatinib as a Sensitizing Agent for Cancer Chemotherapy -- Bosutinib as a Sensitizing Agent for Cancer Chemotherapy -- Bafetinib as a Sensitizing Agent for Cancer Chemotherapy -- Conclusions and Perspectives -- Acknowledgment -- References -- Chapter 3: VEGFR Inhibitors as Sensitizing Agents for Cancer Chemotherapy -- Introduction -- Development of chemotherapeutic Agents -- Tumor Angiogenesis and Tumor Angiogenesis Inhibitors (TAIs) -- Tumor Angiogenesis and VEGF/VEGFR Signaling Pathway -- The Development of TAIs -- Bevacizumab -- Ramucirumab -- Sorafenib -- Other TAIs -- Conclusions -- Acknowledgments -- References -- Chapter 4: ALK Tyrosine Kinase Inhibitors in Drug Sensitization -- Introduction -- ALK Signaling Pathway -- ALK TKIs in Reversing Multidrug Resistance -- Crizotinib -- Ceritinib
- Alectinib -- Lorlatinib -- Perspective -- Acknowledgments -- References -- Chapter 5: STAT3 Inhibitors as Sensitizing Agents for Cancer Chemotherapy -- Introduction -- STAT3 Inhibitors -- STAT3-DNA-Binding Domain Inhibitors -- STAT3 SH2 Domain Inhibitors -- Peptides -- Small Molecules -- Nature Products -- Conclusion -- Acknowledgments -- References -- Further Reading -- Chapter 6: FLT3 Inhibitors as Sensitizing Agents for Cancer Chemotherapy -- FLT3 Mutations in Acute Myeloid Leukemia -- FLT3 Mutations in Other Malignancies -- FLT3-ITD and Drug Resistance -- FLT3 Inhibitors -- First- and Second-Generation FLT3 Inhibitors -- Type I and Type II FLT3 Inhibitors -- Reversal of Drug Resistance by FLT3 Inhibition -- Sequence Dependence of Effects of FLT3 Inhibitor on Chemotherapy Response of Cells With FLT3-ITD -- FLT3 Inhibitors-Current Status -- Role of Off-Target Effects in Chemosensitization by FLT3 Inhibitors -- Drug Transport Proteins in AML -- FLT3-ITD and Expression of Drug Transport Proteins -- Tyrosine Kinase Inhibitor Effects on Drug Transport Proteins -- FLT3 Inhibitor Effects on Drug Transport Proteins -- Midostaurin -- Sunitinib -- Sorafenib -- Ponatinib -- Ibrutinib -- Crenolanib -- Gilteritinib -- Quizartinib -- Conclusions -- Acknowledgments -- References -- Chapter 7: Collagen Signaling in Cancer -- Introduction -- Collagen Types -- Collagen Structure -- Collagens in Normal Physiology and Tumorigenesis -- Collagen Expression in Pancreatic Ductal Adenocarcinoma -- Collagen Function in the PDA -- Collagen Receptors -- DDRs -- Regulation of DDR1 Signaling by Secreted Protein Acidic and Rich in Cysteine -- DDR as a Therapeutic Target -- DDR Inhibitors -- Conclusion -- Acknowledgment -- References -- Chapter 8: Bruton's Tyrosine Kinase (BTK) Inhibitors as Sensitizing Agents for Cancer Chemotherapy -- Introduction
- BTK and BCR Signaling Pathway -- BTK Inhibitors -- Mechanisms of MDR -- BTK Inhibitors in Sensitization of Resistance to Various Chemotherapy Drugs -- BTK Inhibitors Sensitize Cancer Cells Resistant to Paclitaxel -- BTK Inhibitors Sensitize Cancer Cells Resistant to Cisplatin -- BTK Inhibitors Sensitize Cancer Cells Resistant to Doxorubicin -- BTK Inhibitors Sensitize Cancer Cells Resistant to Proteasome Inhibitors -- BTK Inhibitors Sensitize Cancer Cells Resistant to Bcl-2 Antagonists -- BTK Inhibitors Sensitize Cancer Cells Resistant to HDAC Inhibitors -- Discussion -- Conclusions -- Acknowledgment -- References -- Chapter 9: CDK Inhibitors as Sensitizing Agents for Cancer Chemotherapy -- Introduction -- CDKs and Their Regulation of Cell Cycle -- Mechanism of Chemo Sensitization Mediated by CDK4/6 -- CDK4 and 6 Inhibitors as Sensitizing Agents for Cancer Chemotherapy -- First-Generation CDK Inhibitors -- Alvocidib (Flavopiridol) -- UCN-01 (7-Hydroxystaurosporine) -- Seliciclib (Roscovitine) -- Second-Generation CDK Inhibitors -- Palbociclib (PD0332991) -- Ribociclib (LEE011) -- Abemaciclib (LY2835219) -- Dinaciclib (SCH727965) -- AT7519 -- BMS-387032 (SNS-032) -- Riviciclib -- Voruciclib (P1446A) -- CYC065 -- Toxicity of CDK Inhibitors -- Similarities and Differences Between CDK4 and 6 Inhibitors -- Reasons for the Failure of CDK Inhibitors -- Conclusion and Perspective -- Acknowledgments -- References -- Further Reading -- Chapter 10: Bcl-2 Inhibitors as Sensitizing Agents for Cancer Chemotherapy -- Introduction -- Bcl-2 Family Proteins -- Bcl-2 Homology Regions -- Structure and Interactions of Bcl-2 Family Proteins -- Structure -- Interaction Between Antiapoptotic and Proapoptotic Bcl-2 Proteins -- Bcl-2 Proteins Engaged in Apoptosis -- Two Major Apoptotic Pathways -- Roles of Bcl-2 Proteins in Apoptotic Pathway
- Rational for Bcl-2 Inhibitors as Sensitizing Agents -- Overexpression of Bcl-2 in Cancer Patients -- Mechanism of Overexpression of Bcl-2 in Cancers -- Bcl-2-Associated Resistance to Cancer Therapy -- Targeting Bcl-2 for Cancer Therapies Strategy -- Bcl-2 Antisense Oligonucleotide in Cancer Therapy -- Oblimersen (G3139, Genasense) -- Small Molecule Downregulating Gene or Protein Expression of Bcl-2 -- Histone Deacetylase Inhibitor (HDACI), sodium butyrate (NaB), Vorinostat, and Depsipeptide -- Synthetic Retinoid -- Cyclin-Dependent Kinase (CDK) Inhibitors -- BH3 Mimetics -- Levo gossypol (AT101, Ascenta) -- ABT-737(A-779024) and ABT-263 (Navitoclax) -- ABT-199 (Venetoclax) -- S55746 (Bcl201, Servier-1) -- Small Molecule to Targeting Other Antiapoptotic Proteins -- Selective Inhibitors Targeting Bcl-XL Agent, A-1155463, A-1331852, and WEHI-539 -- Selective Anti-Mcl-1 Agents, UMI-177, A-1210477, and AMG176 -- Conclusion -- Acknowledgment -- References -- Further Reading -- Chapter 11: Small Molecule Chemosensitizing Agents: Polo-Like Kinase 1 (Plk1), BRAF and Janus Kinase (JAK) Inhibitors -- Introduction -- Interactions Between MDR-Linked ABC Transporters and PKIs -- Plk1 Inhibitors -- BI 2536 -- Volasertib (BI 6727) -- GSK461364 -- NMS-P937 -- BRAF Inhibitors -- Sorafenib (BAY43-9006) -- Vemurafenib (PLX4032) -- PLX4720 -- Dabrafenib (GSK2118436) -- CEP-32496 -- JAK Inhibitors -- WHI-P154 -- Ruxolitinib (INCB018424) -- Momelotinib (CYT387) -- CEP-33779 -- NVP-BSK805 -- Conclusion -- Acknowledgments -- References -- Further Reading -- Chapter 12: PI3K/AKT Inhibitors as Sensitizing Agents for Cancer Chemotherapy -- The PI3K/AKT Pathway Overview -- The PI3K/Akt Pathway Involved in Diverse Resistances to Chemotherapy -- The PI3K/Akt Pathway Contributes to MDR -- The PI3K/AKT Pathway Contributes to Maintenance of Cancer Stem Cells
- The PI3K/Akt Pathway Contributes to the Resistance to Traditional Cytotoxic Chemotherapy -- The PI3K/AKT Pathway Contributes to the Resistance to RTK Inhibitors -- The PI3K/AKT Pathway Contributes to Resistance to Endocrine Therapy -- The PI3K/Akt Pathway Contributes to Resistance to the RAS/RAF/MAPK Pathway Inhibitors -- The PI3K/Akt Pathway Contributes to Resistance to the Hedgehog Pathway Inhibitors -- The PI3K/Akt Pathway Contributes to Resistance to Proteasome Inhibitors -- The PI3K/Akt Inhibitors as Sensitizing Agents for Cancer Chemotherapy -- Copanlisib -- Idelalisib -- ZSTK474 -- BKM120 -- GDC0941 -- NVP-BEZ235 -- Other PI3K Inhibitors -- AKT Inhibitors as Sensitizing Agents for Cancer Chemotherapy -- Perifosine -- MK2206 -- AZD5363 -- Conclusion -- Acknowledgments -- References -- Chapter 13: Proteasome Inhibitors as Sensitizing Agents for Cancer Chemotherapy -- Introduction -- Bortezomib Combination With Chemotherapy Drugs -- Combination in MM -- Combination in MCL -- Combination in Other Tumors -- Combination of Carfilzomib With Chemotherapeutic Drugs -- Combination of Marizomib With Chemotherapeutic Drugs -- Combination of Ixazomib With Chemotherapeutic Drugs -- Other Proteasome Inhibitors Combination With Chemotherapy Drugs -- Oprozomib, Delanzomib, and MLN-2238 -- Chloroquine -- MG132 -- Gambogic Acid -- Pristimerin -- Conclusions and Perspectives -- Acknowledgments -- References -- Chapter 14: Combining PI3K/Akt/mTOR Inhibition With Chemotherapy -- Introduction -- PI3K/Akt/mTOR Signaling -- Feedback Loops: S6K and PTEN -- PI3K/Akt/mTOR Pathway Activation and Chemotherapy Resistance -- PI3K/Akt/mTOR Inhibitors as Chemosensitizers -- Rapamycin and the Rapalogs -- PI3K Inhibitors -- Dual PI3K/mTOR Kinase Inhibitors -- Dual mTORC1/mTORC2 Inhibitors -- Akt Inhibitors -- Conclusion -- Acknowledgment -- References
- Chapter 15: MDM2/P53 Inhibitors as Sensitizing Agents for Cancer Chemotherapy